TY  - EJOU
AU  - LAN, YU-YAN 
AU  - CHENG, TSUN-CHIH 
AU  - LEE, YI-PING 
AU  - WANG, CHIA-YIH 
AU  - HUANG, BU-MIIN 

TI  - Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways
T2  - BIOCELL

PY  - 2024
VL  - 48
IS  - 7
SN  - 1667-5746

AB  -  <b>Background:</b> Paclitaxel is a compound derived from Pacific yew bark that induces various cancer cell apoptosis. However, whether it also has anticancer activities in KOSC3 cells, an oral cancer cell line, is unclear. <b>Methods:</b> 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and western blotting assays were carried out to assess cell viability, subG1 phase of the cell cycle, and apoptosis-related protein expression, respectively. <b>Results:</b> Our findings indicate that paclitaxel could inhibit cell viability and increase the expression of apoptotic markers, including plasma membrane blebbing and the cleavage of poly ADP-ribose polymerase in KOSC3 cells. Also, the treatment with paclitaxel remarkably elevated the percentage of the subG1 phase in KOSC3 cells. In addition, treatment with a pan-caspase inhibitor could recover paclitaxel-inhibited cell viability. Moreover, caspase-8, caspase-9, caspase-7, and BH3 interacting domain death agonist (Bid) were activated in paclitaxel-treated KOSC3 cells. <b>Conclusions:</b> Paclitaxel induced apoptosis through caspase cascade in KOSC3 cells.
KW  - Paclitaxel; Oral cancer; KOSC3 cells; Apoptosis; Caspase pathways

DO  - 10.32604/biocell.2024.050701